Epicardial Macro-Reentrant Ventricular Tachycardia Exhibiting an Endocardial Centrifugal Activation Pattern in a Case with Arrhythmogenic Right Ventricular Cardiomyopathy

A 55-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent catheter ablation of ventricular tachycardia (VT) with left bundle branch block and left superior axis QRS morphology with an early precordial transition. Endocardial mapping during the VT revealed a focal activation pattern from a small region of low voltage in the left ventricular (LV) septum. Despite earliest endocardial activation in the LV septum, epicardial mapping demonstrated a macro-reentrant circuit with successful catheter ablation at an inferior peritricuspid annular site. Activation from the reentrant circuit propagated through the scar area in the epicardial right ventricle to the remote endocardial LV breakout site.     

The Origin of Epicardial Ventricular Tachycardia Revealed by Entrainment From a Permanent Epicardial Left Ventricular Pacing Lead

Entrainment From Left Ventricular Pacing Lead. Recognizing ventricular tachycardias (VTs) that require epicardial ablation is desirable, but challenging when prior surgery prevents percutaneous epicardial mapping. This patient had cardiomyopathy, prior cardiac surgery, and VT that failed endocardial ablation. Observing that the Bi‐V implantable cardioverter defibrillator (ICD), left ventricular (LV) lead was epicardial to the area of infarct scar, it was used to pace during VT. Entrainment with concealed fusion with long stimulus to QRS interval, consistent with an epicardial VT circuit, was observed. Surgical cryoablation targeting the area around the LV lead eliminated VT. Thus pacing maneuvers from permanent epicardial leads can occasionally help identify an epicardial VT origin. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1293‐1295, November 2010)     

QRS characteristics fail to reliably identify ventricular tachycardias that require epicardial ablation in ischemic heart disease

Criteria for Epicardial Origin in Ischemic VT. Objectives: We tested proposed algorithms for idiopathic and nonischemic tachycardias for their ability to identify epicardial LV‐VT origins. Backgroud: Several ECG features have been reported to identify epicardial origins for left ventricular tachycardias (LV‐VTs) in the absence of myocardial infarction. Only limited data exist in postinfarction patients. Methods: The QRS features of 24 VTs that were ablated from the epicardium and 39 left ventricular VTs ablated from the endocardium were retrospectively analyzed for various 12‐lead ECG features previously reported. Results: No ECG feature consistently predicted an epicardial LV‐VT origin in infarct‐related tachycardias, with epicardial VTs showing slightly longer QRS durations (189 ± 32 ms in epicardial vs 179 ± 37 ms in endocardial, P = 0.28). Pseudo‐delta duration was 38 ± 27 versus 47 ± 27 ms (P = 0.2), intrinsicoid deflection time 93 ± 35 versus 86 ± 32 ms (P = 0.4), shortest RS 97 ± 38 versus 99 ± 32 ms (P = 0.77), and median deflection index 0.82 ± 0.25 versus 0.87 ± 0.22 (P = 0.43). The finding of a Q wave in lead I and the absence of a Q wave in the inferior leads failed to predict an epicardial origin in superior LV‐VT sites. Q waves in any inferior lead and aVR/aVL‐ratio<1 were not specific for an epicardial origin in inferior sites (all P = ns). Furthermore, all inferior LV‐VTs showed a Q wave in the inferior leads which correlated with pre‐existing Q‐waves in sinus rhythm (P = 0.045). Conclusion : Proposed 12‐lead ECG features for differentiation of epicardial versus endocardial sites for nonischemic LV‐VTs do not reliably identify VTs that require ablation from the epicardium. Endocardial mapping should be the first approach to catheter ablation for VTs in patients with ischemic heart disease. (J Cardiovasc Electrophysiol, Vol. 23, pp. 188‐193, February 2012)     

Electrophysiological Mapping and Radiofrequency Catheter Ablation for Ventricular Tachycardia in a Patient with Peripartum Cardiomyopathy

A 38‐year‐old female with prior failed endocardial ablation for ventricular tachycardia (VT) was referred for further treatment. She had been diagnosed with peripartum cardiomyopathy 7 years before and had persistent left ventricular dysfunction with an ejection fraction of 20%. Epicardial voltage mapping showed extensive epicardial scar despite absence of endocardial scar. Five distinct VT morphologies were induced. Ablation was aided by electrogram characteristics, pace mapping, entrainment mapping, and establishing electrical inexcitability along areas of epicardial scar. After epicardial ablation no sustained VT was induced. She had been doing well without VT occurrence but died 1 year later unexpectedly at home.     

Endomyocardial substrate of ventricular arrhythmias in patients with autoimmune rheumatic diseases

Introduction

Delayed enhancement-magnetic resonance imaging (DE-MRI) has demonstrated that nonischemic cardiomyopathy is mainly characterized by intramural or epicardial fibrosis whereas global endomyocardial fibrosis suggests cardiac involvement in autoimmune rheumatic diseases or amyloidosis. Conduction disorders and sudden cardiac death are important manifestations of autoimmune rheumatic diseases with cardiac involvement but the substrates of ventricular arrhythmias in autoimmune rheumatic diseases have not been fully elucidated.

Methods and Results

20 patients with autoimmune rheumatic diseases presenting with ventricular tachycardia (VT) (n = 11) or frequent ventricular extrasystoles (n = 9) underwent DE-MRI and/or endocardial electroanatomical mapping of the left ventricle (LV). Ten patients with autoimmune rheumatic diseases underwent VT ablation. Global endomyocardial fibrosis without myocardial thickening and unrelated to coronary territories was detected by DE-MRI or electroanatomical voltage mapping in 9 of 20 patients with autoimmune rheumatic diseases. In the other patients with autoimmune rheumatic diseases, limited regions of predominantly epicardial (n = 4) and intramyocardial (n = 5) fibrosis or only minimal fibrosis (n = 2) were found using DE-MRI. Endocardial low-amplitude diastolic potentials and pre-systolic Purkinje or fascicular potentials, mostly within fibrotic areas, were identified as the targets of successful VT ablation in 7 of 10 patients with autoimmune rheumatic diseases.

Conclusion

Global endomyocardial fibrosis can be a tool to diagnose severe cardiac involvement in autoimmune rheumatic diseases and may serve as the substrate of ventricular arrhythmias in a substantial part of patients.     

Sinus rhythm ECG criteria associated with basal-lateral ventricular tachycardia substrate in patients with nonischemic cardiomyopathy

ECG Criteria Associated with NICM VT . Introduction: Patients with nonischemic cardiomyopathy (NICM) and ventricular tachycardia (VT) usually have basal‐lateral scar in the left ventricle (LV). We sought to determine electrocardiogram (ECG) characteristics that may help identify NICM patients with basal‐lateral scar and VT. Methods and Results: Phase I, study patients (n = 25) had NICM, VT, and endocardial/epicardial basal‐lateral LV low voltage consistent with scar on detailed mapping. ECGs were compared to controls (n = 18) with NICM, and comparable age and gender without VT/known scar. All patients had either sinus or paced atrial rhythm ECGs without bundle‐branch block or ventricular pacing. In phase II, criteria were evaluated prospectively, blinded to clinical data, using ECGs from 15 NICM patients, of which 7 patients had VT and endocardial/epicardial basal‐lateral LV scar on detailed mapping. Of ECG characteristics studied, V1 R and R:S ratio, and V6 S and S:R ratio were univariately associated with basal‐lateral‐scar associated VT. Controlling for LVEF and multicollinearity in multivariate analyses, V1 R ≥ 0.15 mV (P = 0.001) and V6 S ≥ 0.15 mV (P < 0.001), or V6 S:R ≥ 0.2 mV (P < 0.001), best predicted presence of basal‐lateral scar. In Phase II, the former criteria best identified those with NICM and VT because of basal‐lateral scar, with sensitivity and specificity 0.86 and 0.88, respectively. Conclusions: Among patients with NICM, VT, and normal QRS duration, V1 R ≥ 0.15 mV and V6 S ≥ 0.15 mV predicted presence of basal‐lateral LV areas of bipolar low voltage. This ECG information may have important value in defining presence of LV scar and possible risk for VT in NICM patients. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1351‐1358, December 2011)     

Substrate in the interventricular septum for left ventricular and right ventricular outflow tract tachycardia: ablation from the right side of the septum

Simultaneous epicardial and endocardial mapping demonstrated that in a substantial number of ventricular tachycardias (VTs) endocardial, intramural, and epicardial structures are involved in the substrate of the reentrant circuits. Both right and left ventricular breakthrough has also been described during VT originating in the interventricular septum. We report the case of a patient with a nonischemic left ventricular aneurysm presenting with a left ventricular outflow tract (LVOT) tachycardia and a right ventricular outflow tract (RVOT) tachycardia. Mapping from the anterior interventricular vein and the endocardium of the RVOT revealed mid-diastolic potentials at the epicardium of the LVOT and the endocardium of RVOT, where the criteria of central isthmus sites could be demonstrated. Ablation targeting an isolated late potential during sinus rhythm in RVOT eliminated both the LVOT tachycardia and the RVOT tachycardia. In this patient with a nonischemic left ventricular aneurysm, the substrate of a LVOT tachycardia and RVOT tachycardia is described, and successful catheter ablation of the right and left ventricular tachycardia from the septal wall of RVOT is reported.     

Radiofrequency Ablation Guided by Mechanical Termination of Idiopathic Ventricular Arrhythmias Originating in the Right Ventricular Outflow Tract

Mapping of Idiopathic Ventricular Arrhythmias. Background: Termination of ventricular tachycardia (VT) by mechanical pressure has been described for fascicular and postinfarction VT. Mechanical interruption of idiopathic ventricular arrhythmias (VT/premature ventricular complexes [PVCs]) arising in the right ventricular outflow tract (RVOT) has not been described in systematic fashion. Methods: Eighteen consecutive patients (13 females, age 49 ± 13 years, ejection fraction 0.55 ± 0.12) underwent mapping and ablation of RVOT VT or PVCs. In 7 patients, 9 distinct VTs (mean cycle length 440 ± 127 ms), and in 11 patients, 11 distinct PVCs originating in the RVOT were targeted. Mechanical termination was considered present if a reproducibly inducible VT was no longer inducible or if frequent PVCs suddenly ceased with the mapping catheter at a particular location. Endocardial activation time, electrogram characteristics, and pace‐mapping morphology were assessed at this location. Radiofrequency energy was delivered if mechanical termination was observed. Results: All targeted arrhythmias were successfully ablated. In 7 of 18 patients (39%), catheter manipulation terminated the arrhythmia with the mapping catheter located at a particular site. Local endocardial activation time was earlier at sites of mechanical termination (?31 ± 7 ms) compared with effective sites without termination (?25 ± 3 ms, P = 0.04). The 10‐ms isochronal area was smaller in patients with mechanical interruption (0.35 ± 0.2 cm²) than in patients without mechanical termination (1.33 ± 0.9 cm², P = 0.01). At all sites susceptible to mechanical trauma, the pace map displayed a match with the targeted VT/PVC. All sites where mechanical termination of VT or PVCs occurred were effective ablation sites. Conclusions: Mechanical suppression at the site of origin of idiopathic RVOT arrhythmias frequently occurs during the mapping procedure and is a reliable indicator of effective ablation sites. Mechanical termination of RVOT arrhythmias may be indicative of a more localized arrhythmogenic substrate. (J Cardiovasc Electrophysiol, Vol. 21, pp. 42–46, January 2010)     

Correlation of spatial patterns of endocardial pace mapping to underlying scar topography in patients with scar-related ventricular tachycardia

Introduction

Endocardial pace mapping (PM) can identify conducting channels for ventricular tachycardia (VT) circuits in patients with structural heart disease (SHD). Recent findings show the temporal and spatial pattern of PM may aid identification of the surface harboring VT isthmii. The specific correlation of PM patterns to scar topography has not been examined.

Objective

To correlate the pattern of endocardial PMs to underlying scar topography in SHD patients with VT.

Methods

Data from patients undergoing VT ablation from August 2018 to February 2022 were reviewed.

Results

Sixty-three patients with SHD-related VT (mean age 65 ± 14 years) with 83 endocardial PM correlation maps were analysed. Two main correlation patterns were identified, an “abrupt-change correlation pattern (AC-pattern)” and “centrifugal-attenuation correlation pattern (CA-pattern).” AC-pattern had lower scar ratio (unipolar/bipolar % scar area; 1.1 vs. 1.5, p < .001), had longer maximal stimulus-QRS intervals (97.5 vs. 68 ms, p = .002), and higher likelihood of endocardial dominant scar (11/21 [52%] vs. 3/38 [8%], p < .001) than CA-pattern seen on intracardiac echocardiography (ICE). In contrast, CA-pattern was more likely to have epicardial dominant scar or mid-intramural scar on ICE (epicardial dominant scar; CA-pattern: 12/38 [32%] vs. AC-pattern: 1/21 [5%], p = .02, mid-intramural scar; CA-pattern: 15/38 [39%] vs. AC-pattern: 1/21 [5%], p = .005).

Conclusions

The spatial pattern of endocardial PM in SHD-related VT directly correlates with scar topography. AC-pattern is associated with endocardial dominant scar on ICE with lower scar ratio and longer stimulus-QRS intervals, whereas CA-pattern is strongly associated with epicardial dominant or mid-intramural scar with higher scar ratio and shorter stimulus-QRS intervals.     

Ultra High‐Density Multipolar Mapping With Double Ventricular Access: A Novel Technique for Ablation of Ventricular Tachycardia

Ultra High‐Density Multipolar Mapping With Double Ventricular Access . Background: Analogous to the use of circular loop catheters to guide ablation around the pulmonary veins, it may be advantageous to use a multipolar catheter in the ventricle for rapid mapping and to guide ablation. We describe a technique using double access into the left ventricle for multipolar electroanatomic mapping and ablation of scar‐mediated ventricular tachycardia (VT). Methods: Double access into the left ventricle was obtained via transseptal technique. Endocardial mapping was performed via the first transseptal sheath using a steerable duodecapolar catheter. Higher density mapping was performed in areas of dense scar (<0.5 mV) and border zone (0.5–1.5 mV). All late potentials (LPs) observed on the 20 poles were tagged and pacemapping was performed at these sites for comparison with the clinical or induced VT 12‐lead template. If VT was hemodynamically tolerated, entrainment mapping was attempted at sites demonstrating diastolic activity. Ablation was performed through the second transseptal sheath with an open‐irrigated catheter at target sites identified by LPs, pacemapping, and/or entrainment on the duodecapolar catheter. Results: Seventeen patients (88% ischemic cardiomyopathy) underwent electroanatomic mapping and ablation with double transseptal access. The mean number of endocardial mapping points was 819 ± 357 with an average mapping time of 31 ± 7 minutes. The mean number of VTs induced was 2.8 ± 1.6, mean cycle length 418 ms ± 101. LPs were seen in all patients during endocardial mapping with the duodecapolar catheter. Good (56%) and perfect (44%) pacemaps were seen in all patients when performed. Concealed entrainment, guided by the earliest diastolic activity seen on the duodecapolar catheter, was demonstrated in 4 patients (24%). Acute success was achieved in 94% of patients with complete success in 47% and partial success in 47%. The intermediate success rate (free of VT recurrence) was 69%, with an average follow‐up of 8 ± 3 months. Conclusion: Mapping and ablation of scar‐mediated VT using a multipolar catheter results in ultra high‐density delineation of the left ventricular substrate. A novel double ventricular access strategy has the potential to facilitate identification of LPs, pacemapping, and entrainment mapping. (J Cardiovasc Electrophysiol, Vol. 22, pp. 49‐56, January 2011)     

Electroanatomical Mapping‐Guided Endocardial and Epicardial Ablation of Sustained Ventricular Tachycardia Originating From Alcohol Septal Ablation‐Induced Scar in a Patient With Hypertrophic Obstructive Cardiomyopathy

Ventricular Tachycardia After Alcohol Septal Ablation. A 76‐year‐old female developed 2 different ventricular tachycardias (VTs) 5 years after alcohol septal ablation (ASA) for symptomatic hypertrophic obstructive cardiomyopathy. VT#1 was a small macroreentry at the anterior border of the low‐voltage zone, suggesting the ASA‐scar and eliminated by endocardial ablation at a site recording fractionated potentials covering the mid‐diastolic and presystolic periods. VT#2 was a focal VT and eliminated by epicardial cryoablation at the basal posterior left ventricle, suggesting the posterior border of the ASA‐scar. Using the electroanatomical mapping, we demonstrated that the mechanism of the VTs was reentry at the edge of the ASA‐scar. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1296‐1299, November 2010)     

Magnetic resonance-based anatomical analysis of scar-related ventricular tachycardia: implications for catheter ablation

In catheter ablation of scar-related monomorphic ventricular tachycardia (VT), substrate voltage mapping is used to electrically define the scar during sinus rhythm. However, the electrically defined scar may not accurately reflect the anatomical scar. Magnetic resonance-based visualization of the scar may elucidate the 3D anatomical correlation between the fine structural details of the scar and scar-related VT circuits. We registered VT activation sequence with the 3D scar anatomy derived from high-resolution contrast-enhanced MRI in a swine model of chronic myocardial infarction using epicardial sock electrodes (n=6, epicardial group), which have direct contact with the myocardium where the electrical signal is recorded. In a separate group of animals (n=5, endocardial group), we also assessed the incidence of endocardial reentry in this model using endocardial basket catheters. Ten to 12 weeks after myocardial infarction, sustained monomorphic VT was reproducibly induced in all animals (n=11). In the epicardial group, 21 VT morphologies were induced, of which 4 (19.0%) showed epicardial reentry. The reentry isthmus was characterized by a relatively small volume of viable myocardium bound by the scar tissue at the infarct border zone or over the infarct. In the endocardial group (n=5), 6 VT morphologies were induced, of which 4 (66.7%) showed endocardial reentry. In conclusion, MRI revealed a scar with spatially complex structures, particularly at the isthmus, with substrate for multiple VT morphologies after a single ischemic episode. Magnetic resonance-based visualization of scar morphology would potentially contribute to preprocedural planning for catheter ablation of scar-related, unmappable VT.     

Value of high-density endocardial and epicardial mapping for catheter ablation of hemodynamically unstable ventricular tachycardia

BACKGROUND: Percutaneous epicardial mapping has been used for ablation of recurrent ventricular tachycardia (VT). OBJECTIVES: The purpose of this study was to use a combined epicardial and endocardial mapping strategy to delineate the myocardial substrate for recurrent VT in both ischemic (n = 12) and nonischemic cardiomyopathy (n = 8), and to define the role of epicardial ablation. METHODS: Electroanatomic mapping was performed in 20 patients. High-density voltage maps were obtained by acquiring both endocardial and epicardial electrograms. Electrograms derived from six patients with structurally normal hearts were used as controls. A total of 26 VTs were targeted in the 20 patients. RESULTS: Most VTs (23/26 [88.5%]) were hemodynamically unstable. In patients with ischemic cardiomyopathy, the extent of endocardial scar was greater than epicardial scar. A definable pattern of scar could not be demonstrated in nonischemic cardiomyopathy. Pathologic examination of explanted hearts in two patients with nonischemic cardiomyopathy demonstrated that low-voltage areas were not always predictive of scarred myocardium. A substrate-based approach was used for catheter ablation. Catheter ablation was performed on the endocardium in all patients; additional epicardial delivery of radiofrequency energy was required in 8 (40%) of 20 patients for successful ablation. During follow-up (12 +/- 4 months), 15 (75%) of 20 patients have been arrhythmia-free. CONCLUSION: Patients with ischemic cardiomyopathy tend to have a larger endocardial than epicardial scar. Use of epicardial and endocardial electroanatomic mapping to define the full extent of myocardial scars allows successful catheter ablation in patients with hemodynamically unstable VTs.     

Integration of Merged Delayed‐Enhanced Magnetic Resonance Imaging and Multidetector Computed Tomography for the Guidance of Ventricular Tachycardia Ablation: A Pilot Study

MDCT/MRI Fusion for the Guidance of VT Ablation . Background: Delayed enhancement (DE) MRI can assess the fibrotic substrate of scar‐related VT. MDCT has the advantage of inframillimetric spatial resolution and better 3D reconstructions. We sought to evaluate the feasibility and usefulness of integrating merged MDCT/MRI data in 3D‐mapping systems for structure–function assessment and multimodal guidance of VT mapping and ablation. Methods: Nine patients, including 3 ischemic cardiomyopathy (ICM), 3 nonischemic cardiomyopathy (NICM), 2 myocarditis, and 1 redo procedure for idiopathic VT, underwent MRI and MDCT before VT ablation. Merged MRI/MDCT data were integrated in 3D‐mapping systems and registered to high‐density endocardial and epicardial maps. Low‐voltage areas (<1.5 mV) and local abnormal ventricular activities (LAVA) during sinus rhythm were correlated to DE at MRI, and wall‐thinning (WT) at MDCT. Results: Endocardium and epicardium were mapped with 391 ± 388 and 1098 ± 734 points per map, respectively. Registration of MDCT allowed visualization of coronary arteries during epicardial mapping/ablation. In the idiopathic patient, integration of MRI data identified previously ablated regions. In ICM patients, both DE at MRI and WT at MDCT matched areas of low voltage (overlap 94 ± 6% and 79 ± 5%, respectively). In NICM patients, wall‐thinning areas matched areas of low voltage (overlap 63 ± 21%). In patients with myocarditis, subepicardial DE matched areas of epicardial low voltage (overlap 92 ± 12%). A total number of 266 LAVA sites were found in 7/9 patients. All LAVA sites were associated to structural substrate at imaging (90% inside, 100% within 18 mm). Conclusion: The integration of merged MDCT and DEMRI data is feasible and allows combining substrate assessment with high‐spatial resolution to better define structure–function relationship in scar‐related VT. (J Cardiovasc Electrophysiol, Vol. 24, pp. 419‐426, April 2013)     

Relationship between successful ablation sites and the scar border zone defined by substrate mapping for ventricular tachycardia post-myocardial infarction

INTRODUCTION: It is unknown if identification of scar border zones by electroanatomical mapping correlates with successful ablation sites determined from mapping during ventricular tachycardia (VT) post-myocardial infarction (MI). We sought to assess the relationship between successful ablation sites of hemodynamically stable post-MI VTs determined by mapping during VT with the scar border zone defined in sinus rhythm. METHODS AND RESULTS: Forty-six patients presenting with hemodynamically stable, mappable monomorphic VT post-MI and who had at least one such VT successfully ablated were prospectively included in the study. In each patient, VT was ablated by targeting regions during VT that exhibited early activation, +/- isolated mid-diastolic potentials, and concealed entrainment suggesting a critical isthmus site. Prior to ablation, a detailed sinus-rhythm CARTO voltage map of the left ventricle was obtained. A voltage <0.5 mV defined dense scar. Successful VT ablation sites were registered on the sinus voltage map to assess their relationship to the scar border zone. Of the 86 VTs, 68% were successfully ablated at sites in the endocardial border zone. The remaining VTs had ablation sites within the scar in (18%), in normal myocardium (4%), and on the epicardial surface (10%). There were no significant differences in VT recurrence amongst the different groups. CONCLUSION: Successful ablation sites of hemodynamically stable, monomorphic VTs post-MI are often located in the scar border zone as defined by substrate voltage mapping. However, in a sizable minority, ablation sites are located within endocardial scar, epicardially, and even in normal myocardium.     

Endocardial and Epicardial Ablation Guided by Nonsurgical Transthoracic Epicardial Mapping to Treat Recurrent Ventricular Tachycardia

Nonsurgical Epicardial Ablation. Introduction : An epicardial site of origin of ventricular tachycardia (VT) may explain unsuccessful endocardial radiofrequency (RF) catheter ablation. A new technique to map the epicardial surface of the heart through pericardial puncture was presented recently and opened the possibility of using epicardial mapping to guide endocardial ablation or epicardial catheter ablation. We report the efficacy and safety of these two approaches to treat 10 consecutive patients with VT and Chagas' disease.
Methods and Results : Epicardial mapping was carried out with a regular steerable catheter introduced into the pericardial space. An epicardial circuit was found in 14 of 18 mapable VTs induced in 10 patients. Epicardial mapping was used to guide endocardial ablation in 4 patients and epicardial ablation in 6. The epicardial earliest activation site occurred 107 ± 60 msec earlier than the onset of the QRS complex. At the epicardial site used to guide endocardial ablation, earliest activation occurred 75 ± 55 msec before the QRS complex. Epicardial mid-diastolic potentials and/or continuous electrical activity were seen in 7 patients. After 4.8 ± 2.9 seconds of epicardial RF applications, VT was rendered noninducible. Hemopericardium requiring drainage occurred in 1 patient; 3 others developed pericardial friction without hemopericardium. Patients remain asymptomatic 5 to 9 months after the procedure. Interruption during endocardial pulses occurred after 20.2 ± 14 seconds (P = 0.004), hut VT was always reinducible and the patients experienced a poor outcome.
Conclusion : Epicardial mapping does not enhance the effectiveness of endocardial pulses of RF. Epicardial applications of RF energy can safely and effectively treat patients with VT and Chagas' disease.     

Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 +/- 3 days following experimental myocardial infarction were placed on total cardiopulmonary bypass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43-62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.     

Noncontact mapping to guide ablation of right ventricular outflow tract tachycardia

OBJEWCTIVES: The aim of this study was to determine whether noncontact mapping is feasible in the right ventricle and assess its utility in guiding ablation of difficult-to-treat right ventricular outflow tract (RVOT) ventricular tachycardia (VT). BACKGROUND: In patients without inducible arrhythmia, RVOT VT may be difficult to ablate. Noncontact mapping permits ablation guided by a single tachycardia complex, which may facilitate ablation of difficult cases. However, the mapping system may be geometry-dependent, and it has not been validated in the unique geometry of the RVOT. METHODS: Ten patients with left bundle inferior axis VT, no history of myocardial infarction and normal left ventricular function underwent noncontact guided ablation; seven had failed previous ablation and three had received a defibrillator. All noncontact maps were analyzed by a blinded reviewer to determine whether the arrhythmia focus was epicardial and to predict on the basis of the map whether arrhythmia would recur. RESULTS: The procedure was acutely successful in 9 of 10 patients. During a mean follow-up of 11 months, 7 of 9 patients remained arrhythmia-free. Both patients in whom the blinded reviewer predicted failure had arrhythmia recurrence: one due to epicardial origin with multiple endocardial exit sites and one due to discordance between site of lesion placement and earliest activation on noncontact map. CONCLUSIONS: Mechanisms of ablation failure in RVOT VT include absence of sustained arrhythmia, difficulty with substrate localization and epicardial origin of arrhythmia. In this study, noncontact mapping was safely and effectively used to guide ablation of patients with difficult-to-treat RVOT VT.     

Ventricular Tachycardia After Myocardial Infarction: From Arrhythmia Surgery to Catheter Ablation

Ablation of Ventricular Tachycardia. Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits arc diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendo-cardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8%, at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can he mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.     

Repeat percutaneous epicardial mapping and ablation of ventricular tachycardia: safety and outcome

Safety and Efficacy of Repeat Epicardial Access. Introduction: Epicardial mapping and ablation of ventricular tachycardia (VT) has been increasingly performed. Occasionally additional ablation is necessary, requiring repeat percutaneous access to the pericardial space. Methods and Results: We studied 30 consecutive patients who required a repeat epicardial procedure. We specifically examined the success and safety of repeat percutaneous pericardial access as well as the ability to map and ablate epicardial VT targets. Percutaneous pericardial access at a median of 110 days after the last procedure was successful in all 30 patients. Significant adhesions interfering with catheter mapping were encountered in 7 patients (23%); 6 had received intrapericardial triamcinolone acetate (IPTA) with prior procedures. Using blunt dissection with a deflected ablation catheter and a steerable sheath, adhesions were divided allowing for complete catheter mapping in 5 patients with areas of dense adherence compartmentalizing the pericardium in 1 patient and precluding ablation over previously targeted ablation site in the second. Targeted VT noninducibility was achieved in 27 (90%) patients including 7 patients with adhesions. No direct complications related to pericardial access or adhesions disruption occurred. One periprocedural death occurred from refractory cardiogenic shock in patient with LV ejection fraction of 10%. Another patient developed asymptomatic positive Haemophilus influenzae pericardial fluid cultures identified at second procedure, which was successfully treated. Conclusions: Repeat access can be obtained after prior epicardial ablation. Adhesions from prior procedures may limit mapping, but can usually be disrupted mechanically and allow for ablation of recurrent VT. IPTA may not completely prevent adhesions. (J Cardiovasc Electrophysiol, Vol. 23, pp. 744‐749, July 2012)